From said study: "In this prospective study we found that serum IgG4 level predicts a poor COVID-19 outcome. Based on the available literature, IgG4 antibodies may contribute to COVID-19 progression . . . ."
The patients in this study had Covid between June and December 2020, prior to the rollout of the mRNA vaccines. So, my first (of several) questions is: how and why are certain individuals producing IgG4 antibodies?
Hopefully Brian will weigh in on this (which, is another example of why I suggested some posts on the whole phenomenon (see my comment below).
"The mRNA-vaccinated appear to be stuck with their original B Cell pool forever." You said that in your "Updates to Invincible imprinting...." (which, BTW, I tried to post this comment/question but it wouldn't let me unless I was a paid subscriber (I've just been tipping you via Kofi)).
So what are your thoughts on the whole autophagy thing in regards to B cells and the IgG4 phenomenon? Can autophagy (specifically, obtained by regular fasting) "reset" or "clear" the B cell pool of a mRNA-vaccinated individual by killing off B cells?
Thanks for the heads up! - I don't know how I managed to only fix one of the defaults since it's very easy to remember that there are two to fix. It's a very annoying feature.
I can't say. But if so, it wouldn't matter much unless for some reason it killed off specific cells and clones, namely IgG4 ones, which would change the ratio. Otherwise when spike is encountered and the B Cell pool expands, it doesn't matter if there are a different number of clone phenotypes because the IgG4 ratio will be the same. So it's like if you started deleting duplicate adjectives from the English language at random, would people use a different ratio of nice and mean words? Probably not.
Generally, B Cells dwindle on their own. And some clonal lineages do "disappear" over time anyway, but maybe this means that they dwindle to a very few cells and can expand again if they are a better match for a variant. Either way they are like a compressed file waiting to be expanded again if the virus comes back.
Suggestion: it would be good to have someone like yourself do a post (or posts) on the ramifications of the IgG class switching phenomenon--to explore what that means for (or what will happen to) the 2x+ mRNA jabbed and to what extent or distribution (e.g. what possible scenarios are likely to play out and their odds of happening). I'm observing a broad spectrum of responses to the discovery of it. On the one extreme, some are predicting bad things for the 2x+ jabbed: IgG4 related diseases (autoimmunity, etc.), maiming of organs, constant covid infections, etc. On the other extreme, some are saying the IgG4 switch is a nothing burger: IgG4 antibodies still neutralize and the tolerance is actually a good thing b/c it is reducing inflation, etc.
I recognize there is not enough studies and/or understanding about the matter, but I believe we should begin assessing and discussing the possible prognoses so that those who are 2x+ jabbed can be better prepared.
I would say, probably no one offering the "tolerance reduces inflammation / over-response" take has interrogated the actual support for the cytokine storm meme. It's basically a myth. It was never the problem. In severe infections, the virus turns your lungs into soup, the immune response is not the problem - and immune response is relatively suppressed compared to flu https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7725462/
If neutralization were enough for viruses, why would immunity build in all these extra functions (effects) into antibodies? Why would our blood be soaked with complement at all times, to prompt auto-destruction of cells that multiple IgG1 antibodies attach to? IgG4 turns all of that off (just one IgG4 can block complement from an IgG1 complex. So, I don't think there's grounds for saying "no biggie."
The first report about placental transfer of COVID-19 vaccine-induced antibodies from the mother to the twin fetuses: https://mdpi.com/2076-393X/11/1/116
- Antibody levels in both twins were approx. 2 times higher than those in the mother
- In one twin, IgG4 increased more than in the mother
I'm not following this part : "Addetia, et al. did not look at IgG4; but they did poke around to see how well donor plasma bound to “FcγRIIIa.” This is essentially asking plasma how well it will theoretically tell Natural Killer and T Cells to destroy cells that have spike protein."
According to wikipedia, the FCfancyRIIIA binds to antibodies in a non-specific manner. So why does this result above tell us anything about the response to spike? Is it to be interpreted that the plasma from different people just had different levels of antibodies, which we are assume are antibodies to spike?
The anti-spike antibodies in the plasma are either inferred to be high based on high neutralization performance or were separately measured as well, I forget. They’re probably high and probably sticking to the spike expressing cells. But then this other molecule doesn’t also stick. This molecule looks for the other IgG types that says kill this cell. It doesn’t bind IgG4. So the low scores probably mean high IgG4.
Oh boy... dots connecting alert. I just watched this video that has lots of UK-based doctors stating their reservations about the mRNA vaccines. Starting at about 3:40 an Oncologist states that "after the booster" 7, or 8 of his patients that he had been caring for long term and that were in a controlled state had relapses that were "aggressive". The IgG4 is affecting more than just Covid-19 relapses...
DoorlessCarp says "In this author’s view by Karagiannis et al from 2013 the inhibitory but non-neutralising effects of IgG4 antibodies on melanoma are discussed."
From the paper; "The role of B cells and antibodies in cancer is insufficiently understood but is receiving increasing attention. We have recently identified IgG4 as an antibody subclass elicited by melanoma-associated interleukin-10-driven inflammation. In this setting, IgG4 exhibit inefficient immunostimulatory capacity and block the cytotoxic activities of other antibodies. These previously unappreciated mechanisms of immune escape may constitute promising targets for the development of novel anticancer immunotherapies."
So my point is not necessarily that the spike-specific IgG4 antibodies are directly inducing turbo melanoma, but rather that the signaling mechanisms (IL-10?) that underlie the IgG4 spike response may also benefit the growth of melanoma in this way. I am trying to put a mechanistic framework to the oncologist's observation of 7-8 patients that had their well-controlled melanoma become aggressive only after booster. This is a VERY specific observation, and we know that IgG4 blooms especially AFTER BOOSTER. This is not a coincidence. I can see the pattern, but I don't have the depth in immunology to tie up the mechanism....
edit;
Or maybe the spike IgG4 is the problem.. more from the same post by Doorlesscarp;
"In 2020, Wang et al found a correlation between IgG4, esophageal cancer, metastasis and poor prognosis27.......... Antigen specificity was not a requirement either:"
From the paper:
Results: In a cohort of patients with esophageal cancer we found that IgG4-containing B lymphocytes and IgG4 concentration were significantly increased in cancer tissue and IgG4 concentrations increased in serum of patients with cancer. Both were positively related to increased cancer malignancy and poor prognoses, that is, more IgG4 appeared to associate with more aggressive cancer growth. We further found that IgG4, regardless of its antigen specificity, inhibited the classic immune reactions of antibody-dependent cell-mediated cytotoxicity, antibody-dependent cellular phagocytosis and complement-dependent cytotoxicity against cancer cells in vitro, and these effects were obtained through its Fc fragment reacting to the Fc fragments of cancer-specific IgG1 that has been bound to cancer antigens. We also found that IgG4 competed with IgG1 in reacting to Fc receptors of immune effector cells. Therefore, locally increased IgG4 in cancer microenvironment should inhibit antibody-mediated anticancer responses and help cancer to evade local immune attack and indirectly promote cancer growth.
Once again, from the above paragraph; .... "IgG4, REGARDLESS OF ITS ANTIGEN SPECIFICITY...."
Piggybacking on Jim H's comment below. Isn't he basically describing Typhoid Mary? Obviously we don't have data from that era, but an asymptomatic carrier of a infection (in Typhoid's case a bacteria) that the body tolerates? Typhoid bacterium in non-tolerant individuals causes the full immune response including the characteristic fever and rash, whereas it is plausible that Mary Mallon and other asymptomatic carriers had reached an IgG4 tolerance or response? Typhoid typically infects the skin though so it would explain possibly why Mary and others didn't die from the bacteria unlike a virus which may eventually lead to viremia and then organ failure. Also the successful melanoma drug Nivolumab basically prevents IgG4 response to cancer cells in the skin. It would be interesting if perhaps unethical and unlikely to look for asymptomatic Typhoid carriers where Typhoid still occurs and see if they do indeed have this "tolerant" response.
Typhoid Mary is an interesting case. We now know that we all have loads of "pathogenic" bacteria in us all the time, as long as they are part of a balanced microbiome, it is fine. So there's not really any way to have someone be a "vector" by virtue of having more of salmonella without symptoms, I think she was just really bad at washing her hands... At all events all she had to do was stop getting jobs as a cook and she wouldn't have kept being found, haha.
Of course, none of the BA.1 infected died. Do we know if any of them got severely ill? I ask, as I see two options:
1) The fact that no new specific B-cells/antibodies are made and existing transform to IgG4 doesn't matter, as there were enough IgG1 left.
2) The fact that no new specific B-cells/antibodies are made and existing transform to IgG4 DID matter, and the individual got severely sick.
What I wonder if how many of the e.g. Moderna + BA.1 (footnote 8) study were in category 2. If all were in category 1, I'd not be too worried.
But if any were in category 2, meaning that even after the body struggled fighting off the BA.1, and still refused to adapt, that would literally be OAS ... Francis would then deserve a cookie after all :-)
Also in this context, didn't we also establish close to 100% of all covid-after-vax survivors produce N-antibodies provided one waits long enough? N-antibodies may be less effective, but N-CD8+ killer cells are! In fact after natural infection, it was established that typically at least 50% of CD8+ T cells were N-triggered, not spike or RBD.
OAS is set of claims about a design "flaw" of the immune system. The mRNA injections can't validate that claim because they use two exposures. Besides the unnatural prolonging of exposure and the removal of PAMPS context, etc. Anyway OAS basically says "You can't make antibodies to new variants; the antibodies you make to new variants are just old antibodies remodeled" which has no clear valence. Which thing is supposed to be falsified? That is the point, it's meant to be a motte and bailey.
I would bring up 3) They had mild or moderate infections, and the virus is still simmering away in their body at the time of the draw, with potential organ failure emerging at some point. That's the tolerance maims theory.
Exactly, immune responses to N will emerge and compensate for IgG4 cellular immune suppression, to some extent. It's a question of whether some people can't stamp out the virus no matter what, and how often that happens, we have no idea yet.
Yes, OAS suggests a flaw. I think you have proven OAS does not exist in the context of it being a flaw for natural infections. The 'old' antibodies after all work fine.
But what about unnatural meddling with our immune system by usage of protein stimulants? Both (2) and (3) seem a form of OAS as in the old antibodies do NOT work fine. That does seem like a "flaw", as I'd hope/expect the body feedback mechanisms would eventually find out it "ain't working" and start creating new ones. But perhaps a simmering doesn't trigger enough IgM's vs a more pseudo-exponential growth?
Also if they can stamp out N-antibodies, why not spike/RBD antibodies for the parts that are unique? There seems to be no difference in the IgM 'learning' mechanism after all. Perhaps small mutations won't trigger enough IgM?
But either way, this then does seem a form of OAS, be it not in the way Francis believed, nor in the 'OAS' is innocent imprinting.
But your theory does seem interesting. If true, I'd expect some people to semi-chronically test positive, right? Especially with PCR being so good a testing fragments, you'd have to find some trace of such a simmering.
Also, do you have any idea how often the spike protein from the mRNA shots crosses the BBB? There's that one study from Japan that found spike in the brain. Other than that, it doesn't seem like anyone has been looking. Although, it was shown back in 2020 that SP crosses the BBB (in mice, but still).
Right, that paper has been online for a while I believe. Quotes Tetz and Tetz, everyone keeps quoting Tetz and Tetz on that but they didn't use the tool correctly. Humans don't actually have insight into how prions work but we can train algorithms on fungus prions and the spike protein doesn't have a domain. It would just be flagged at the bottom of a list of 1,00,000 proteins if you were using the tool to search for potential prion domains.
Regarding vax in brain, I think it's probably going there, but the effects seem to be mysterious as is often the case with the brain. I had a weird observation of a person having brain fog for the entire time after their first course, and then it went away after the booster.
There was definitely a brain element to the infection. Might be anecdotal, but I was first infected during summer 2021. The preceeding sensations were immense brain fog and suprisingly the sensations that I have previously known from an antidepressant withdrawal - The infamous "brain zaps". Plus the sense of smell disappearing for about a year, and then coming back altered. Anyway, maybe someone finds this observation useful.
Is there any neurologists that has weighted in on these vaccine/Covid induced damages? Some of the videos of the collapsing/dying suddenly are a far cry from cardiological reaction. The folks seem to be knocked out to be honest, not trying to sit down, clutching left arm etc. as would be expected if there is still pressure and oxygen in the cardiovascular system. And the "Pfizer roll" torso twist seems vertebrobasillar or cerebellar.
But I try to stick with the simplest model for everything. I haven't seen a neurologist make a theory. There's lots of autonomic disruption with both Long Covid and (presumably) Long Vaccine.
Thank you Brian.. I can feel my T-cells mood improving now that we are back to the real time immunology. Speaking of immunology, how exactly did these mRNA lackeys from Canada manage to skew their results in favor of hybrid immunity, especially given everything you have just explained about the limitations of injected "immunity"?
Here is the headline Yahoo used in promoting the study;
Recovering from COVID doesn’t give you bulletproof immunity—’hybrid’ immunity is way better, according to a new WHO study
Oh, reviews - I hate reviews. Could they have done anything other than trawl a bunch of test-negative studies for worthless results?... Nope there it is, 65% test-negative studies so, just a lot of nonsense mixed together
Invited Commentary: Beware the Test-Negative Design
.....While confounding and measurement error are common in observational studies, the potential for selection bias inherent in the test-negative design brings into question the validity of inferences drawn from such studies.
Bias can be an issue. More-so, it's just not a rational design. All it tells you is that more of one group showed up for a test wrongly, ie had the symptoms but not the virus. So you can easily imagine that Covid vaccines will look better here by imitating symptoms and driving tests, boom, more vaxxed in the negative group.
Another example is the 2009 pdmH1N1 / swine flu. Lots of test negative studies purport to show that vaccine increased how often you got swine flu. In fact it was just decreasing how often you got the other flu (the one you were vaxxed for), so there were fewer negative vaxxed. So it's crazy that anyone is even allowed to publish studies using test negative, they just create falsehoods.
The missing piece in all of this is no repeat infection for unvaccinated people, but we probably will never get such a study.
If we assume spike alone is the culprit that puts us in a precarious situation.
We may suggest that the mRNAs are just producing far too many spike (with missing features of HOW exactly), but the mRNA having greater spike production feels like a given. But if it's constant exposure to spike alone that sort of makes us wonder about all of the constant spike that we are all exposed to, especially if we are to assume that many of the vaccinated are supposed to be spewing spike (something I'm still very hesitant about).
In a previous thread I had pointed to this paper, which shows an HIV vaccine using a dissociated (gp120) protein sequence failing in efficacy and in fact inducing IgG4.
Noting: "One component of the RV144 vaccine, the AIDSVAX B/E bivalent rgp120 protein, was also given with alum in seven doses in the VAX003 phase 3 vaccine trial"
My contention is that our immune systems may know the difference between being hit with proteins from a viral or bacterial pathogen vs nuisance food-based or other allergen proteins by some signal relating to the fragment profiles. The injection of disconnected viral proteins, in both cases (the HIV trial, and the newer mRNA's) may be fooling our ability to discriminate.
I would also say, the immune system has a few viral proteins that it will "innately" mount a strong (memory) response to, like flu HAs, even in a dead virus injection. And with proteins that it doesn't, then there is no point trying to push it. This is essentially the whole Sisyphean task of HIV vaccines for the last 2 decades, they are trying to make HIV "sexy" but the immune system doesn't find it interesting before infection. At which point there's already tolerance building.
(This is probably fine with natural, low doses of the virus - it is just like any other dormancy-capable virus that colonizes our immune cells throughout life - which is why we never noticed it before even though it is almost certainly an ancient human virus like every other virus turns out to be. Then we figured out a way (two ways) to give each other high doses of the virus, and gather a lot of people with high doses together so the pattern was noticeable, and voila "epidemic." That's my current theory. I hope I'll be able to start posting about the bug more this year.)
Of course, age of exposure almost certainly has an influence on this as well. Adults might be less responsive to things you could successfully trick kids' immune systems into responding to. But that's not always the case, with the spike protein there's no big difference in adults and kids to injected exposure.
I think it's just worth it given the context of supposed aerosolized spike from the vaccinated. If we are to assume that to be the case, then we should inherently assume that everyone is likely to experience IgG4 subclass conversion, but that's also why I'm hesitant of the aerosolized spike given the limited evidence because it just seems to fit too well into the doomsday position.
By constant "exposure to spike" and "aerosolized spike," do you mean spike shedding?
If so, I tend to agree with Brian--IgG4 conversion is not something the unvaccinated need to worry about.
In order for B cells to churn out anti-spike IgG antibodies, the body would have to be "infected" with lots of spike antigen for a long time (7 days?), if it even gets past the innate immune system. What is more, IgM and IgA abs will be the first line of defense against spike and should adequately handle the amounts of aerosolized or shedded spike that might get past the innate arm. So, IgG B cells will probably never be called upon.
Quick anecdote. Last January I (unvaxxed) got omicron from a boostered individual (LOL). Thereafter, whenever I hung out with said individual, I experienced sick/cold symptoms (sort throat, congestion, etc.) but said symptoms would go away after a few days. Upon re-exposure to this person, I would experience sick/cold symptoms again. This process repeated itself several times. I concluded it was some sort of shedding phenomena going on. A month later, I got a Covid antibodies test. Result: IgG abs was negative. So, after getting Covid and being exposed to a boostered individual, there wasn't enough spike in me to make IgG abs, let alone produce a class shift.
IgG4 formation is dose dependent in the vax'ed. Do you really think that secondary exposure, likely sans engineered lipid nanoparticle coating, would be enough to register?
Why be concerned about so called variants when the message is loud and clear since more than a year if it was not so before then, that the mRNA shots will not prevent expression of the Covid-19 symptoms nor possible transmission to others. In addition since the earliest days of the rollout, worldwide evidence was gathering quickly and giving a strong signal that multiple shots may lead to severe depression of the body's ability to deal with ANY invasive pathogen, even to near zero capability in an AIDS like condition.
Quantification of the mRNA-vaccine-induced-IgG4 mortality risk:
The mRNA vaccinated with 2+ doses have nearly 3x higher COVID-19 fatality rate than people with low IgG4 antibody levels
Please read here in detail: https://massimaux.substack.com/p/serum-igg4-level-increased-with-mrna
Very interesting!
From said study: "In this prospective study we found that serum IgG4 level predicts a poor COVID-19 outcome. Based on the available literature, IgG4 antibodies may contribute to COVID-19 progression . . . ."
The patients in this study had Covid between June and December 2020, prior to the rollout of the mRNA vaccines. So, my first (of several) questions is: how and why are certain individuals producing IgG4 antibodies?
Hopefully Brian will weigh in on this (which, is another example of why I suggested some posts on the whole phenomenon (see my comment below).
"The mRNA-vaccinated appear to be stuck with their original B Cell pool forever." You said that in your "Updates to Invincible imprinting...." (which, BTW, I tried to post this comment/question but it wouldn't let me unless I was a paid subscriber (I've just been tipping you via Kofi)).
So what are your thoughts on the whole autophagy thing in regards to B cells and the IgG4 phenomenon? Can autophagy (specifically, obtained by regular fasting) "reset" or "clear" the B cell pool of a mRNA-vaccinated individual by killing off B cells?
Thanks for the heads up! - I don't know how I managed to only fix one of the defaults since it's very easy to remember that there are two to fix. It's a very annoying feature.
I can't say. But if so, it wouldn't matter much unless for some reason it killed off specific cells and clones, namely IgG4 ones, which would change the ratio. Otherwise when spike is encountered and the B Cell pool expands, it doesn't matter if there are a different number of clone phenotypes because the IgG4 ratio will be the same. So it's like if you started deleting duplicate adjectives from the English language at random, would people use a different ratio of nice and mean words? Probably not.
Generally, B Cells dwindle on their own. And some clonal lineages do "disappear" over time anyway, but maybe this means that they dwindle to a very few cells and can expand again if they are a better match for a variant. Either way they are like a compressed file waiting to be expanded again if the virus comes back.
Makes sense. Thanks!
Suggestion: it would be good to have someone like yourself do a post (or posts) on the ramifications of the IgG class switching phenomenon--to explore what that means for (or what will happen to) the 2x+ mRNA jabbed and to what extent or distribution (e.g. what possible scenarios are likely to play out and their odds of happening). I'm observing a broad spectrum of responses to the discovery of it. On the one extreme, some are predicting bad things for the 2x+ jabbed: IgG4 related diseases (autoimmunity, etc.), maiming of organs, constant covid infections, etc. On the other extreme, some are saying the IgG4 switch is a nothing burger: IgG4 antibodies still neutralize and the tolerance is actually a good thing b/c it is reducing inflation, etc.
I recognize there is not enough studies and/or understanding about the matter, but I believe we should begin assessing and discussing the possible prognoses so that those who are 2x+ jabbed can be better prepared.
I would say, probably no one offering the "tolerance reduces inflammation / over-response" take has interrogated the actual support for the cytokine storm meme. It's basically a myth. It was never the problem. In severe infections, the virus turns your lungs into soup, the immune response is not the problem - and immune response is relatively suppressed compared to flu https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7725462/
If neutralization were enough for viruses, why would immunity build in all these extra functions (effects) into antibodies? Why would our blood be soaked with complement at all times, to prompt auto-destruction of cells that multiple IgG1 antibodies attach to? IgG4 turns all of that off (just one IgG4 can block complement from an IgG1 complex. So, I don't think there's grounds for saying "no biggie."
I did do "maims and kills" explaining some of my thoughts, not too in detail https://unglossed.substack.com/p/tolerance-maims-and-kills-potential
That's kinda what I was thinking. Thanks for the response!
Dr John B tells us that IgG4 now comes in newborn baby size! Thanks Mom!
https://twitter.com/DrJohnB2/status/1617082835570941954
The first report about placental transfer of COVID-19 vaccine-induced antibodies from the mother to the twin fetuses: https://mdpi.com/2076-393X/11/1/116
- Antibody levels in both twins were approx. 2 times higher than those in the mother
- In one twin, IgG4 increased more than in the mother
Looks like it's just trace IgG4, in line with it not being mRNA shots
I totally missed this comment
I'm not following this part : "Addetia, et al. did not look at IgG4; but they did poke around to see how well donor plasma bound to “FcγRIIIa.” This is essentially asking plasma how well it will theoretically tell Natural Killer and T Cells to destroy cells that have spike protein."
According to wikipedia, the FCfancyRIIIA binds to antibodies in a non-specific manner. So why does this result above tell us anything about the response to spike? Is it to be interpreted that the plasma from different people just had different levels of antibodies, which we are assume are antibodies to spike?
The anti-spike antibodies in the plasma are either inferred to be high based on high neutralization performance or were separately measured as well, I forget. They’re probably high and probably sticking to the spike expressing cells. But then this other molecule doesn’t also stick. This molecule looks for the other IgG types that says kill this cell. It doesn’t bind IgG4. So the low scores probably mean high IgG4.
Oh boy... dots connecting alert. I just watched this video that has lots of UK-based doctors stating their reservations about the mRNA vaccines. Starting at about 3:40 an Oncologist states that "after the booster" 7, or 8 of his patients that he had been caring for long term and that were in a controlled state had relapses that were "aggressive". The IgG4 is affecting more than just Covid-19 relapses...
https://www.bitchute.com/video/RRDtH4xLnXtL/
Saw that. It was interesting how the focus was so much on boosters with older doctors, and intrinsic risks with younger doctors.
Thanks Brian.. I do want to be more specific though in terms of my thinking.
There is a connection between IgG4 and melanoma;
https://doorlesscarp953.substack.com/p/spike-protein-inc-vax-induced-immunodeficiency-819
DoorlessCarp says "In this author’s view by Karagiannis et al from 2013 the inhibitory but non-neutralising effects of IgG4 antibodies on melanoma are discussed."
From the paper; "The role of B cells and antibodies in cancer is insufficiently understood but is receiving increasing attention. We have recently identified IgG4 as an antibody subclass elicited by melanoma-associated interleukin-10-driven inflammation. In this setting, IgG4 exhibit inefficient immunostimulatory capacity and block the cytotoxic activities of other antibodies. These previously unappreciated mechanisms of immune escape may constitute promising targets for the development of novel anticancer immunotherapies."
So my point is not necessarily that the spike-specific IgG4 antibodies are directly inducing turbo melanoma, but rather that the signaling mechanisms (IL-10?) that underlie the IgG4 spike response may also benefit the growth of melanoma in this way. I am trying to put a mechanistic framework to the oncologist's observation of 7-8 patients that had their well-controlled melanoma become aggressive only after booster. This is a VERY specific observation, and we know that IgG4 blooms especially AFTER BOOSTER. This is not a coincidence. I can see the pattern, but I don't have the depth in immunology to tie up the mechanism....
edit;
Or maybe the spike IgG4 is the problem.. more from the same post by Doorlesscarp;
"In 2020, Wang et al found a correlation between IgG4, esophageal cancer, metastasis and poor prognosis27.......... Antigen specificity was not a requirement either:"
From the paper:
Results: In a cohort of patients with esophageal cancer we found that IgG4-containing B lymphocytes and IgG4 concentration were significantly increased in cancer tissue and IgG4 concentrations increased in serum of patients with cancer. Both were positively related to increased cancer malignancy and poor prognoses, that is, more IgG4 appeared to associate with more aggressive cancer growth. We further found that IgG4, regardless of its antigen specificity, inhibited the classic immune reactions of antibody-dependent cell-mediated cytotoxicity, antibody-dependent cellular phagocytosis and complement-dependent cytotoxicity against cancer cells in vitro, and these effects were obtained through its Fc fragment reacting to the Fc fragments of cancer-specific IgG1 that has been bound to cancer antigens. We also found that IgG4 competed with IgG1 in reacting to Fc receptors of immune effector cells. Therefore, locally increased IgG4 in cancer microenvironment should inhibit antibody-mediated anticancer responses and help cancer to evade local immune attack and indirectly promote cancer growth.
Once again, from the above paragraph; .... "IgG4, REGARDLESS OF ITS ANTIGEN SPECIFICITY...."
Piggybacking on Jim H's comment below. Isn't he basically describing Typhoid Mary? Obviously we don't have data from that era, but an asymptomatic carrier of a infection (in Typhoid's case a bacteria) that the body tolerates? Typhoid bacterium in non-tolerant individuals causes the full immune response including the characteristic fever and rash, whereas it is plausible that Mary Mallon and other asymptomatic carriers had reached an IgG4 tolerance or response? Typhoid typically infects the skin though so it would explain possibly why Mary and others didn't die from the bacteria unlike a virus which may eventually lead to viremia and then organ failure. Also the successful melanoma drug Nivolumab basically prevents IgG4 response to cancer cells in the skin. It would be interesting if perhaps unethical and unlikely to look for asymptomatic Typhoid carriers where Typhoid still occurs and see if they do indeed have this "tolerant" response.
Typhoid Mary is an interesting case. We now know that we all have loads of "pathogenic" bacteria in us all the time, as long as they are part of a balanced microbiome, it is fine. So there's not really any way to have someone be a "vector" by virtue of having more of salmonella without symptoms, I think she was just really bad at washing her hands... At all events all she had to do was stop getting jobs as a cook and she wouldn't have kept being found, haha.
Of course, none of the BA.1 infected died. Do we know if any of them got severely ill? I ask, as I see two options:
1) The fact that no new specific B-cells/antibodies are made and existing transform to IgG4 doesn't matter, as there were enough IgG1 left.
2) The fact that no new specific B-cells/antibodies are made and existing transform to IgG4 DID matter, and the individual got severely sick.
What I wonder if how many of the e.g. Moderna + BA.1 (footnote 8) study were in category 2. If all were in category 1, I'd not be too worried.
But if any were in category 2, meaning that even after the body struggled fighting off the BA.1, and still refused to adapt, that would literally be OAS ... Francis would then deserve a cookie after all :-)
Also in this context, didn't we also establish close to 100% of all covid-after-vax survivors produce N-antibodies provided one waits long enough? N-antibodies may be less effective, but N-CD8+ killer cells are! In fact after natural infection, it was established that typically at least 50% of CD8+ T cells were N-triggered, not spike or RBD.
OAS is set of claims about a design "flaw" of the immune system. The mRNA injections can't validate that claim because they use two exposures. Besides the unnatural prolonging of exposure and the removal of PAMPS context, etc. Anyway OAS basically says "You can't make antibodies to new variants; the antibodies you make to new variants are just old antibodies remodeled" which has no clear valence. Which thing is supposed to be falsified? That is the point, it's meant to be a motte and bailey.
I would bring up 3) They had mild or moderate infections, and the virus is still simmering away in their body at the time of the draw, with potential organ failure emerging at some point. That's the tolerance maims theory.
Exactly, immune responses to N will emerge and compensate for IgG4 cellular immune suppression, to some extent. It's a question of whether some people can't stamp out the virus no matter what, and how often that happens, we have no idea yet.
Yes, OAS suggests a flaw. I think you have proven OAS does not exist in the context of it being a flaw for natural infections. The 'old' antibodies after all work fine.
But what about unnatural meddling with our immune system by usage of protein stimulants? Both (2) and (3) seem a form of OAS as in the old antibodies do NOT work fine. That does seem like a "flaw", as I'd hope/expect the body feedback mechanisms would eventually find out it "ain't working" and start creating new ones. But perhaps a simmering doesn't trigger enough IgM's vs a more pseudo-exponential growth?
Also if they can stamp out N-antibodies, why not spike/RBD antibodies for the parts that are unique? There seems to be no difference in the IgM 'learning' mechanism after all. Perhaps small mutations won't trigger enough IgM?
But either way, this then does seem a form of OAS, be it not in the way Francis believed, nor in the 'OAS' is innocent imprinting.
But your theory does seem interesting. If true, I'd expect some people to semi-chronically test positive, right? Especially with PCR being so good a testing fragments, you'd have to find some trace of such a simmering.
Have you seen the CJD paper? I thought there wasn't a prion-forming part of the spike, just amyloidogenic...
https://www.researchgate.net/publication/367167725_Emergence_of_a_New_Creutzfeldt-Jakob_Disease_26_Cases_of_the_Human_Version_of_Mad-Cow_Disease_Days_After_a_COVID-19_Injection
Also, do you have any idea how often the spike protein from the mRNA shots crosses the BBB? There's that one study from Japan that found spike in the brain. Other than that, it doesn't seem like anyone has been looking. Although, it was shown back in 2020 that SP crosses the BBB (in mice, but still).
Right, that paper has been online for a while I believe. Quotes Tetz and Tetz, everyone keeps quoting Tetz and Tetz on that but they didn't use the tool correctly. Humans don't actually have insight into how prions work but we can train algorithms on fungus prions and the spike protein doesn't have a domain. It would just be flagged at the bottom of a list of 1,00,000 proteins if you were using the tool to search for potential prion domains.
But lots of theoretical prion interactions from the RNA itself. Also, since it seems like the transfections code for mutant spikes (https://joomi.substack.com/p/what-proteins-are-we-actually-getting), anything is possible in that regard.
Regarding vax in brain, I think it's probably going there, but the effects seem to be mysterious as is often the case with the brain. I had a weird observation of a person having brain fog for the entire time after their first course, and then it went away after the booster.
There was definitely a brain element to the infection. Might be anecdotal, but I was first infected during summer 2021. The preceeding sensations were immense brain fog and suprisingly the sensations that I have previously known from an antidepressant withdrawal - The infamous "brain zaps". Plus the sense of smell disappearing for about a year, and then coming back altered. Anyway, maybe someone finds this observation useful.
I had two days of fog after Omicron. Would not want it permanently. But, what's life without a little danger.
Is there any neurologists that has weighted in on these vaccine/Covid induced damages? Some of the videos of the collapsing/dying suddenly are a far cry from cardiological reaction. The folks seem to be knocked out to be honest, not trying to sit down, clutching left arm etc. as would be expected if there is still pressure and oxygen in the cardiovascular system. And the "Pfizer roll" torso twist seems vertebrobasillar or cerebellar.
Typically a "heart attack," lack of blood to a part of the heart, precedes cardiac arrest, but if you go straight to cardiac arrest then you get what we have seen with dying suddenly, just dropping. https://www.gvh.org/heart-attack-vs-sudden-cardiac-arrest-know-the-signs/
So I think when it comes to post-myocarditis deaths, we would see what we have seen. It's not a circulation problem. The heart just stops. https://unglossed.substack.com/p/notes-on-sudden-cardiac-deaths
But I try to stick with the simplest model for everything. I haven't seen a neurologist make a theory. There's lots of autonomic disruption with both Long Covid and (presumably) Long Vaccine.
Love the dialog in this post. Even my children can understand the story. (Pretty impressive especially since they are grown).
Thank you Brian.. I can feel my T-cells mood improving now that we are back to the real time immunology. Speaking of immunology, how exactly did these mRNA lackeys from Canada manage to skew their results in favor of hybrid immunity, especially given everything you have just explained about the limitations of injected "immunity"?
Here is the headline Yahoo used in promoting the study;
Recovering from COVID doesn’t give you bulletproof immunity—’hybrid’ immunity is way better, according to a new WHO study
https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(22)00801-5/fulltext
Oh, reviews - I hate reviews. Could they have done anything other than trawl a bunch of test-negative studies for worthless results?... Nope there it is, 65% test-negative studies so, just a lot of nonsense mixed together
Thank you Brian - I have seen you mention this before. I am trying to learn. Do you agree with these authors that the main problem is selection bias?
https://pubmed.ncbi.nlm.nih.gov/27587722/
Am J Epidemiol
. 2016 Sep 1;184(5):354-6. doi: 10.1093/aje/kww063.
Invited Commentary: Beware the Test-Negative Design
.....While confounding and measurement error are common in observational studies, the potential for selection bias inherent in the test-negative design brings into question the validity of inferences drawn from such studies.
Bias can be an issue. More-so, it's just not a rational design. All it tells you is that more of one group showed up for a test wrongly, ie had the symptoms but not the virus. So you can easily imagine that Covid vaccines will look better here by imitating symptoms and driving tests, boom, more vaxxed in the negative group.
Another example is the 2009 pdmH1N1 / swine flu. Lots of test negative studies purport to show that vaccine increased how often you got swine flu. In fact it was just decreasing how often you got the other flu (the one you were vaxxed for), so there were fewer negative vaxxed. So it's crazy that anyone is even allowed to publish studies using test negative, they just create falsehoods.
The missing piece in all of this is no repeat infection for unvaccinated people, but we probably will never get such a study.
If we assume spike alone is the culprit that puts us in a precarious situation.
We may suggest that the mRNAs are just producing far too many spike (with missing features of HOW exactly), but the mRNA having greater spike production feels like a given. But if it's constant exposure to spike alone that sort of makes us wonder about all of the constant spike that we are all exposed to, especially if we are to assume that many of the vaccinated are supposed to be spewing spike (something I'm still very hesitant about).
For now I am not worried about the hypothetical of over-exposure tolerance in unvaccinated even though it is hypothetically valid
In a previous thread I had pointed to this paper, which shows an HIV vaccine using a dissociated (gp120) protein sequence failing in efficacy and in fact inducing IgG4.
https://www.researchgate.net/publication/260950633_Polyfunctional_Fc-Effector_Profiles_Mediated_by_IgG_Subclass_Selection_Distinguish_RV144_and_VAX003_Vaccines
Noting: "One component of the RV144 vaccine, the AIDSVAX B/E bivalent rgp120 protein, was also given with alum in seven doses in the VAX003 phase 3 vaccine trial"
My contention is that our immune systems may know the difference between being hit with proteins from a viral or bacterial pathogen vs nuisance food-based or other allergen proteins by some signal relating to the fragment profiles. The injection of disconnected viral proteins, in both cases (the HIV trial, and the newer mRNA's) may be fooling our ability to discriminate.
I would also say, the immune system has a few viral proteins that it will "innately" mount a strong (memory) response to, like flu HAs, even in a dead virus injection. And with proteins that it doesn't, then there is no point trying to push it. This is essentially the whole Sisyphean task of HIV vaccines for the last 2 decades, they are trying to make HIV "sexy" but the immune system doesn't find it interesting before infection. At which point there's already tolerance building.
(This is probably fine with natural, low doses of the virus - it is just like any other dormancy-capable virus that colonizes our immune cells throughout life - which is why we never noticed it before even though it is almost certainly an ancient human virus like every other virus turns out to be. Then we figured out a way (two ways) to give each other high doses of the virus, and gather a lot of people with high doses together so the pattern was noticeable, and voila "epidemic." That's my current theory. I hope I'll be able to start posting about the bug more this year.)
Of course, age of exposure almost certainly has an influence on this as well. Adults might be less responsive to things you could successfully trick kids' immune systems into responding to. But that's not always the case, with the spike protein there's no big difference in adults and kids to injected exposure.
I think it's just worth it given the context of supposed aerosolized spike from the vaccinated. If we are to assume that to be the case, then we should inherently assume that everyone is likely to experience IgG4 subclass conversion, but that's also why I'm hesitant of the aerosolized spike given the limited evidence because it just seems to fit too well into the doomsday position.
By constant "exposure to spike" and "aerosolized spike," do you mean spike shedding?
If so, I tend to agree with Brian--IgG4 conversion is not something the unvaccinated need to worry about.
In order for B cells to churn out anti-spike IgG antibodies, the body would have to be "infected" with lots of spike antigen for a long time (7 days?), if it even gets past the innate immune system. What is more, IgM and IgA abs will be the first line of defense against spike and should adequately handle the amounts of aerosolized or shedded spike that might get past the innate arm. So, IgG B cells will probably never be called upon.
Quick anecdote. Last January I (unvaxxed) got omicron from a boostered individual (LOL). Thereafter, whenever I hung out with said individual, I experienced sick/cold symptoms (sort throat, congestion, etc.) but said symptoms would go away after a few days. Upon re-exposure to this person, I would experience sick/cold symptoms again. This process repeated itself several times. I concluded it was some sort of shedding phenomena going on. A month later, I got a Covid antibodies test. Result: IgG abs was negative. So, after getting Covid and being exposed to a boostered individual, there wasn't enough spike in me to make IgG abs, let alone produce a class shift.
Thanks for the detailed description of what you experienced and the possible antibody-level explanation Ohio. It all sounds very plausible.
IgG4 formation is dose dependent in the vax'ed. Do you really think that secondary exposure, likely sans engineered lipid nanoparticle coating, would be enough to register?
Brian, please be so kind to have a layman's summary of your posts.
Summary added, thanks.
Noted. Everything important was carefully marked up on figures for rapid consumption without textual disorder.
Why be concerned about so called variants when the message is loud and clear since more than a year if it was not so before then, that the mRNA shots will not prevent expression of the Covid-19 symptoms nor possible transmission to others. In addition since the earliest days of the rollout, worldwide evidence was gathering quickly and giving a strong signal that multiple shots may lead to severe depression of the body's ability to deal with ANY invasive pathogen, even to near zero capability in an AIDS like condition.
The reason for being interested is given in the Context part.
So basically the equivalent of allergy shots....they've desensitized the population to covid. Wonderful.
All these people can still catch covid,
They can still spread covid,
And it continues to damage their organs (unlike allergy shots which only desensitize you from something harmless like pollen).
People have been turned into ticking tome bombs of death.
Walking weapons of mass destruction.
Well, put a psychopath in charge and that's what you get.
Pretty much the deal!
So when approximately would be the time to dress in rags, grow a beard and start carrying arround "the end is near" transparents?